Pressure ulcers (also known as “bed sores” or “pressure sores”) are typically associated with individuals having compromised mobility or lack of sensation, such as the infirm, elderly and people suffering from stroke, spinal cord injury, bone and joint disease, vascular pathologies, tumours and diabetes. People in intensive care units, hospital wards, or undergoing long surgical procedures are also at risk of developing pressure ulcers.
A pressure ulcer is a tissue abnormality or lesion resulting from pressure imposed upon soft tissue underlying skin, fat, fascia, muscle, bone, or any combination thereof. Following prolonged periods of loading (e.g., compression and shear), the soft tissue positioned between a bony prominence (e.g. the ischial tuberosities, trochanter, shoulder blades, sacrum) and an external surface (e.g. bed, wheelchair) begins to break down or deform. Soft tissue breakdown results from the occlusion of capillaries and ischemic reduction of blood flow (i.e. a reduction of oxygen, nutrients, and removal of metabolic waste products) to the loaded tissue region.
Ischemia, therefore, has historically been considered a major factor leading to pressure ulcer formation. Paradoxically, the restoration of blood flow, vital to preserving tissue viability, has also been identified to cause extended damage of the tissue. In addition to the injury caused by biochemical changes occurring during tissue ischemia and ensuing reperfusion, high stress levels at the bone-muscle interface and the duration of their application have also been reported to be direct causes of tissue injury. Furthermore, injury to the muscle result in the formation of scar tissue, thus creating more foci for increased stress and leading to injury of adjacent previously healthy tissue. It is the combined effects of these processes that cause the edema, inflammation and necrosis that ultimately leads to the formation of a pressure ulcer.
Pressure ulcers can be initiated at the dermis, usually in the presence of excessive friction and/or compromised dermal integrity, and progress inwardly towards the deeper layers of tissue (“outside-in ulcers”). Alternatively, pressure ulcers can be initiated in the deep tissue, such as at the site of the bone-muscle interface, and evolve outwardly forming a severe pressure ulcer encompassing damage to muscle, fat and skin. Such ulcers, known as “inside-out ulcers”, result from muscle breakdown due to prolonged pressure causing sustained and damaging mechanical deformation of muscle and ischemic reduction in blood flow to the tissue.
Muscle is considered to be more susceptible than dermis to tissue degradation from mechanical loading and oxygen deprivation. The National Pressure Ulcer Advisory Panel defines inside-out pressure-related injury to deep tissue under intact skin as “deep tissue injury” (DTI). Unlike outside-in ulcers, non-invasive and clinically viable methods for early detection of DTI currently do not exist, to our knowledge. In present clinical practice, pressure ulcers are normally detected by visual inspection of the skin, which often belies existing extensive damage occurring in deeper tissue. Therefore, DTI can be perilous, as it can develop and evolve undetected by the patient or care giver until a significant destruction of the tissue has already occurred.
Current techniques employed to prevent inside-out and outside-in pressure ulcer formation include frequent repositioning of the patient, and the use of specialized cushions and mattresses that provide some pressure relief of the tissues at risk. However, effective administration of these pressure-relieving techniques is difficult, expensive and often dependent upon patient compliance. Repositioning of patients must achieve prolonged pressure relief to the tissue and must be performed either by hospital staff or by encouraging the patient to perform wheelchair push-ups or side-to-side leans. Specialized mattresses and cushions are heavy, expensive and not widely utilized. Further, these techniques merely provide passive tissue load reduction, thereby failing to actively engage the patient's own muscles.
Electrical stimulation of muscle tissue, commonly referred to as electrical muscle stimulation or “EMS”, has been examined as a means for preventing pressure ulcer formation and DTI. For example, EMS treatment has been used with the objectives of:                1. Increasing muscle mass (bulk) in atrophied muscle, thereby improving the cushioning capacity of the muscle, or,        2. Relieving pressure, albeit intermittently, by inducing “lifting” movements of loaded muscles (i.e. inducing changes in seating interface pressure distribution).EMS to Build Muscle Mass        
Having regard to the first technique, EMS may be used as an exercise modality to increase the muscle mass of a particular muscle or muscle group. For example, in order to build mass, EMS may be used to stimulate contraction of a muscle during a “work-out” session (i.e. up to one hour per day), wherein the target muscle is continuously contracted or “activated” for a brief duration (i.e. 5 seconds) and then relaxed or “deactivated” for a brief rest period (i.e. 5 seconds) for the duration of the work-out session. Following daily work-out sessions for prolonged periods (i.e. for up to ˜3 months), increases in muscle mass can be achieved. Increases in muscle mass provide greater cushioning capacity of the muscle and passively improve the static distribution of pressure around bony prominences. Patients receiving treatment in this manner have been shown to be capable of withstanding longer durations in a wheelchair than previously possible due to their atrophied muscles.
As with specialized cushions or mattresses, however, one primary disadvantage of this technique is that any benefits gained during EMS treatment of the loaded muscle (e.g., increase in muscle mass) are abolished when the work-out sessions are discontinued. In addition, in order for the treatment to be effective in reducing pressure sores, the target muscle or muscle groups must be capable of generating minimum threshold forces without becoming fatigued during the work-out. When the fatigued muscle can no longer contract, the work-out must be discontinued and the beneficial effects of the treatment are lost.
Pre-conditioning of the muscle prior to treatment has been utilized as a means of increasing fatigue resistance, thereby enabling the muscle to withstand longer bouts of treatment. As with building muscle mass, however, pre-conditioning can be a laborious task necessitating that electrical stimulation be applied to the muscle daily for several months immediately prior to commencing treatment.
There is a need, therefore, for a treatment that provides effective reduction in DTI pressure sores that does not fatigue the muscle.
EMS to Induce Lifting
Having regard to the second technique, EMS may be used to mimic the temporary relief in pressure that is achieved when a patient is repositioned. It is known that EMS applied directly to the loaded muscle may be utilized to change the shape of that muscle (Levine et al., 1990, Archives of Physical Med & Rehab, 71:210-215). One main disadvantage of this technique, however, is that individuals who suffer from sustained and appreciable muscle atrophy still require prolonged EMS stimulation or pre-conditioning for lifting treatment of the loaded muscle to be effective.
In an alternative approach, EMS may be applied to the muscles surrounding the loaded muscle. One technique involves applying EMS to the muscles around a patient's hips or knee, such as the quadriceps muscles (Ferguson AC. et al., 1992, Paraplegia, 30(7) 474-478), or hamstring muscles (Kaplan HM, et al., 2006, 11th Annual Conference of the International FES Society Proceedings, 112-114), to effect lifting of the (loaded) buttocks from the seating surface. In this approach, however, the patient must be securely stabilized (i.e. restrained) on the seating surface to effectively induce lifting of the target muscle from the seating surface. Further, where EMS is applied to muscles other than those muscles that are directly loaded due to sitting, the patient should be in a seated position and be strapped to the seating surface during treatment. The patient's legs may also be restrained such that when the quadriceps or hamstrings are stimulated to lift the buttocks, lifting movement at the hip is enabled, but movement around the primary joint (i.e. the knee) is prevented. Such restraint of the patient can lead to complications associated with reduced stability of the wheelchair user and/or fracture of weak bones.
There is a need, therefore, for an EMS treatment that does not require pre-conditioning or “lifting” of the loaded muscle.
Despite the foregoing attempts to use unloading or EMS, no single treatment has succeeded in preventing pressure ulcers effectively. The incidence rates of pressure ulcers remain as high as they were nearly half a century ago. Recognizing the absence of a significant reduction in the incidence of pressure ulcers, new preventative interventions are needed, especially for DTI.